From PsychonautWiki
Jump to navigation Jump to search
Summary sheet: MDMA
Chemical Nomenclature
Common names MDMA, Molly, Mandy, Emma, MD, Ecstasy, E, X, XTC, Rolls, Beans, Pingers
Substitutive name 3,4-Methylenedioxy-N-methylamphetamine
Systematic name (RS)-1-(Benzo[d][1,3]dioxol-5-yl)-N-methylpropan-2-amine
Class Membership
Psychoactive class Stimulant / Entactogen
Chemical class Amphetamine / MDxx
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold 20 mg
Light 20 - 80 mg
Common 80 - 120 mg
Strong 120 - 150 mg
Heavy 150 mg +
Total 3 - 6 hours
Onset 30 - 45 minutes
Come up 15 - 30 minutes
Peak 1.5 - 2.5 hours
Offset 1 - 1.5 hours
After effects 12 - 48 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Protease Inhibitors
Serotonin releasers

3,4-Methylenedioxymethamphetamine (also known as ecstasy, E, XTC, emma, molly, mandy, pingers, and MDMA) is a classical entactogen substance of the amphetamine class. It is the most well-known and widely-used member of the entactogens, a diverse group that includes MDA, methylone, 4-MMC, and 6-APB. It produces its effects by promoting the release of serotonin, dopamine, and norepinephrine in the brain, particularly serotonin.

MDMA was first developed in 1912 by the pharmaceutical company Merck.[1] However, human use was not reported until the 1970s, when it became known to underground psychotherapy circles in the United States.[2] In the early 1980s, it spread into nightlife and rave culture, which eventually resulted in federal scheduling in 1985.[3] By 2014, it was estimated to be one of the most popular recreational drugs in the world, alongside cocaine and cannabis.[4]

Today, recreational MDMA use is widely associated with dance parties, electronic dance music, and the clubbing and raving scenes.[5] Researchers are currently investigating whether MDMA may assist in treatment-resistant post-traumatic stress disorder (PTSD), social anxiety in autistic adults,[6] and anxiety in those with life-threatening illness.[7][8][9]

Subjective effects include stimulation, anxiety suppression, disinhibition, enhanced empathy and sociability, relaxation, and euphoria. It is classified as an entactogen due to how it facilitates feelings of closeness with one's self and others. A notable property of MDMA is that tolerance builds unusually quickly and many users report that it dramatically loses effectiveness if used on a frequent basis.

It is usually recommended to wait for one to three months between each use to give the brain adequate time to restore serotonin levels and avoid toxicity. Additionally, using excessively high doses and multiple redosing is highly discouraged as this is thought to significantly increase the toxicity of MDMA.

MDMA has moderate to high abuse potential but a conversely low potential for a genuine psychological dependence or addiction which appears even lower than cannabis (lower than 10%). Interestingly, MDMA’s potential for overuse and dependence or addiction can actually be greatly influenced by certain geographical components such as in other cultures or subcultures similarly to ketamine. Although ketamine‘s addiction potential is still notably higher across various cultures then compared to MDMA. Acute adverse effects of MDMA are usually the result of high amounts or multiple doses; either when done too frequently or excessively within a 24 hour period. Although single dose toxicity can still occur in susceptible individuals.[10] The most serious short-term physical health risks of MDMA are overheating and dehydration, which has resulted in deaths.[11] It has also been shown to be neurotoxic at high doses;[12] however, it is unclear how much this risk applies to typical recreational usage.[13] MDMA may cause excessive thirst, and inability to urinate the water, which may cause water intoxication and electrolyte imbalance. MDMA has been shown to cause sexual dysfunction, including erectile dysfunction and delayed orgasm (see subjective effects).

It is highly advised to use harm reduction practices if using this substance.

History and culture

Patent Certificate for Merck's synthesis of MDMA, dated 1912

MDMA was first synthesized in 1912 by the German chemist Dr. Anton Köllisch while employed at the pharmaceutical company Merck. Köllisch was in the process of developing agents that would help manage excess bleeding and was interested in MDMA synthesis because it was an intermediate in the production of methylhydrastinin, the methylated analog of the hemostatic agent hydrastinine. There are no indications of interest in MDMA as an active agent itself.[1]

It was not mentioned again until 1927, when Dr. Max Oberlin conducted the first proven pharmacological tests at Merck while searching for compounds with a similar action spectrum to adrenaline or ephetonine. Despite promising results, research was halted due to rising substance prices.[1]

In 1965, the American chemist Alexander Shulgin synthesized MDMA as an academic exercise but did not test it for psychoactivity.[14][2] Shulgin claims to have first heard about the effects of MDMA in 1967 from a student and decided to experiment with it himself. He was impressed with the effects of the substance and believed it could have therapeutic utility. He advertised it to therapists and psychiatrists which led it to gain some popularity as an adjunct treatment for various psychological disorders.[2]

During this period, psychotherapist Dr. Leo Zeff came out of retirement and subsequently introduced the then-legal MDMA to over 4,000 patients. From the mid-1970s to the mid-1980s there was a growth of clinicians using MDMA (then known as "Adam") in California.[15]

Recreational use of MDMA became popular at around the same time, particularly in nightclubs, eventually catching the attention of the Drug Enforcement Administration (DEA). After several hearings, a US Federal Administrative Law Judge recommended that MDMA should be made a Schedule III controlled substance so that it could be used in the medical field. Despite this, the director of the DEA overruled this recommendation and classified MDMA as a Schedule I controlled substance.[16][14]

In the United Kingdom, the 1971 Misuse of Drugs Act, which had already been altered in 1977 to include all ring-substituted amphetamines like MDMA, was further amended in 1985 to refer specifically to Ecstasy, placing it in the Class A category.[15]


MDMA, or 3,4-methylenedioxy-N-methylamphetamine, is a synthetic molecule of the substituted amphetamine class. Molecules of the amphetamine class all contain a phenethylamine core comprised of a phenyl ring bound to an amino (NH2) group through an ethyl chain, with an additional methyl substitution at Rα. In addition to this, MDMA contains a methyl substitution on RN, a feature it shares with methamphetamine. Critically, the MDMA molecule also contains substitutions at R3 and R4 of the phenyl ring with oxygen groups -- these oxygen groups are incorporated into a methylenedioxy ring through a methylene bridge. MDMA shares this methylenedioxy ring with other entactogens and stimulants like MDA, MDEA and MDAI.


MDMA acts primarily as a releasing agent of the three principal monoamine neurotransmitters serotonin, norepinephrine, and dopamine through its action at trace amine-associated receptor 1 (TAAR1) and vesicular monoamine transporter 2 (VMAT2).[17][18][19] MDMA is a monoamine transporter substrate (i.e. a substrate for the transporters for dopamine (DAT), norepinephrine (NET), and serotonin (SERT)), enabling it to enter monoaminergic neurons via these neuronal membrane transport proteins.[18] By acting as a monoamine transporter substrate, MDMA produces competitive reuptake inhibition at the neuronal membrane transporters, competing for endogenous monoamines for reuptake.[18][20]

MDMA inhibits both vesicular monoamine transporters (VMATs), the second of which (VMAT2) is highly expressed within monoamine neurons vesicular membranes.[19] Once inside a monoamine neuron, MDMA acts as a VMAT2 inhibitor and a TAAR1 agonist.[18][21] The inhibition of VMAT2 by MDMA results in increased concentrations of the aforementioned monoamine neurotransmitters in the cytosol of the neuron.[19][22] Activation of TAAR1 by MDMA triggers protein kinase signaling events which then phosphorylates the associated monoamine transporters of the neuron.[18]

Subsequently, these phosphorylated monoamine transporters either reverse transport direction – i.e. move neurotransmitters from inside the cell to the synaptic cleft – or withdraw into the neuron, respectively producing the inflow of neurotransmitters and noncompetitive reuptake inhibition at the neuronal membrane transporters.[18] MDMA has ten times more affinity for uptake at serotonin transporters compared to dopamine and norepinephrine transporters and consequently has mainly serotonergic effects.[23]

MDMA also has weak agonist activity at postsynaptic serotonin receptors 5-HT1 and 5-HT2 receptors, and its more efficacious metabolite MDA likely augments this action.[24][25][26][27] Cortisol, prolactin, and oxytocin quantities in serum are increased by MDMA.[28]

Additionally, MDMA is a ligand at both sigma receptor subtypes, though its efficacies at these receptors and the role that they play have yet to be elucidated.[29]

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects

Visual effects

Cognitive effects

Auditory effects

Transpersonal effects

After effects
Aftereffects (3).svg

Dose-effects relationship from analyzed samples

The optimal single oral dose for an average user may be around 90 mg going by this diagram. Note that the percentages at the bottom are too outdated to guide in estimating substance content in current pills: The average concentration of MDMA in ecstasy pills, tested in a drug checking program in Zurich, doubled between 2010 and 2018. The percentage of pills containing more than 120 mg MDMA rose from 4% to 73%. In the same period, the rate of pills containing other psychoactive compounds dropped from 53% to 7%.[44]


Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Names and forms


MDMA pills, commonly called Ecstasy
Off-white MDMA crystals, commonly called Molly

Since the 1980s, MDMA has become widely known as "Ecstasy" (shortened to "E", "X", or "XTC"), usually referring to its street forms as illicitly pressed pills or tablets.[46] The American term "Molly" and the British equivalent term "Mandy" originally referred to crystal or powder MDMA that was purported to be of high purity and free of adulteration.[47] However, it has since evolved into a generic street term for any number of euphoric stimulants that are sold in powder or crystal form.[citation needed]


MDMA can be found in the following forms:


Crystals or powder (commonly called Molly) is a white to brownish substance which can be dissolved, crushed, put into gel capsules or edible paper ("parachutes"). It can be administered orally, sublingually, buccally or via insufflation ("snorting" or "sniffing").


Skull and crossbones darktextred2.png

Do not trust underground brand names, they are easily falsified

The previously good reputation of 'Mistubishi's' amongst ecstasy-users has been dealt a blow with the discovery of deadly batches (PMA has been found in White Mitsubishi,[48] PMMA has been found in Red Mitsubishi[49])

Pills are the most common form in which MDMA is sold, and are commonly referred to as Ecstasy. They often contain other substances or adulterants that range from anything from MDA, MDEA, amphetamine, methamphetamine, caffeine, 2C-B or mCPP to synthesis by-products such as MDP2P, MDDM or 2C-H. They can also contain an array random substances such as research chemicals, prescription drugs, over-the-counter drugs, poisons or nothing at all. It is strongly recommended to take harm reduction measures such as using a reagent testing kit when ingesting unknown pills.
The average concentration of MDMA in ecstasy pills, tested in a drug checking program in Zurich, doubled between 2010 and 2018. The percentage of pills containing more than 120 mg MDMA rose from 4% to 73%. In the same period, the rate of pills containing other psychoactive compounds dropped from 53% to 7%.[50]


MDMA-assisted psychotherapy


Common dosages for MDMA-assisted therapy:

  • 1.1-1.7 mg/kg, or 80-120 mg for a 70 kg person.
  • Kilo body weight + 50 in milligrams

MDMA-assisted psychotherapy for PTSD

In 2011, a pilot study on 20 patients demonstrated promising results in the treatment of post-traumatic stress disorder (PTSD). After two or three MDMA-assisted psychotherapy sessions, 83% of the patients no longer met the criteria for PTSD, compared to only 25% in the control group where MDMA was replaced with a placebo. The results sustained at two and twelve months after the treatment. The MDMA and placebo group both received non-drug psychotherapy before and after the sessions. In the study, a dose of 125mg MDMA plus a 62.5mg supplemental dose after 2 hours have been administered.[51] After completion of the study, the patients from the placebo group also received MDMA-assisted psychotherapy, and a long-term follow-up study of 19 patients published in 2013 shows that even after three years the positive results maintained.[51]

In 2017, the FDA granted MDMA a breakthrough therapy designation for PTSD, meaning if studies show promise, a review for potential medical use could occur more quickly.[52] Phase 3 clinical trials to look at effectiveness and safety have already begun, and are expected to be completed in 2021, meaning the FDA could approve treatment as early as 2022.[53] [54]


MDMA is typically produced and consumed in its racemic form (known as SR-MDMA) which consists of equal parts S-MDMA and R-MDMA. A 2017 study found that high doses of R-MDMA administered in mice increased prosocial behavior and facilitated fear-extinction learning but did not produce hyperthermia or signs of neurotoxicity. This is thought to owe itself to the lower dopamine release R-MDMA displays relative to SR-MDMA. This result suggests that R-MDMA may be a safer and more viable therapeutic than racemic MDMA.[55] However, more research is needed to validate this finding.

Reagent results

Exposing compounds to the reagents gives a colour change which is indicative of the compound under test.

Marquis Mecke Mandelin Liebermann Froehde Gallic
Purple - Black Green - Blue / Black Purple / Blue - Black Intense brown - Black Yellow/green - Dark blue Green to brown
Robadope Ehrlich Hofmann Simon’s Zimmermann Scott Folin
No reaction No reaction No reaction Dark blue No reaction No reaction Orange

Toxicity and harm potential

Table from the 2010 ISCD study ranking various drugs (legal and illegal) based on statements by drug-harm experts. MDMA ("Ecstacy") was found to be the 16th overall most dangerous drug.[56]
Radar plot showing relative physical harm, social harm, and dependence of MDMA[57]

The short-term physical health risks of MDMA consumption include dehydration, bruxism, insomnia, hyperthermia,[58][59] and hyponatremia.[60] MDMA generally does not cause any serious or life threatening effects by itself unless it is associated with other extraneous factors such as exposure to prolonged high ambient temperature and humidity, prolonged physical activities, poor intake of water and lack of acclimatization.[61]

Continuous activity without sufficient rest or rehydration may cause the user's body temperature to rise to dangerous levels, and loss of fluid via excessive sweating puts the body at further risk as the stimulating and euphoric qualities of MDMA may cause the user to become oblivious to their physical condition.

Diuretics such as alcohol may exacerbate these risks further due to causing excessive amounts of dehydration. Users are advised to pay close attention to their water intake, drinking neither too much nor too little, and to take care not to overexert themselves to avoid heat-stroke, which can be fatal.

Toxic dose

The exact toxic dosage is unknown, but considered to be far greater than its effective dose.[citation needed]

Water intoxication and electrolyte imbalance

Water intoxication symptoms typically show up when a person consumes more than about 3-4 liters of water within an hour.[62][63] Also, an important cause of death following MDMA use is hyponatremia, low blood sodium levels as a result of drinking too much water.

Ecstasy users have reported that xerostomia (dry mouth) is common.[64][65] The excessive drinking observed in case reports of MDMA use may be caused by hyperpyrexia, a change in the primary drive to drink, and exposure to harm reduction messages that emphasize the need to drink water.[66] Higher doses of MDMA result in an overall difficulty when it comes to urination.[67] Urinary retention is caused by MDMA’s promotion of the release of anti-diuretic hormone (ADH); ADH is responsible for regulating urination. This effect can be lessened by relaxing, but can also be relieved by placing a hot flannel over the genitals to encourage blood flow.[68][69] However, MDMA causes water retention and dilution of electrolytes. Consequently, overhydration has caused death from water intoxication.[70] It was a main cause of the Death of Leah Betts who consumed an excstasy tablet followed by approximately 7 litres (1.8 US gal) of water in a 90 minute period, that resulted in water intoxication and hyponatremia, which in turn led to serious swelling of the brain, irreparably damaging it.

Users may experience signs of dehydration such as dry mouth and sweating while dancing or in a hot environment.

Water intoxication and electrolyte imbalance prevention

It is advised that users have hydration available, drink to thirst and never over-drink.[citation needed]

  • Avoid consuming more than 3 liters of water within a few hours.
  • Hyponatremia is preventable by drinking fluid containing sodium, such as that contained in sports drinks (typically ~20mM NaCl).


The neurotoxicity of MDMA use is the subject of considerable debate. Scientific study has resulted in the general agreement that, although it is physically safe to try in a responsible context, the administration of repeated or high dosages of MDMA is most certainly neurotoxic in some form.

Administration of MDMA causes subsequent down-regulation of serotonin reuptake transporters in the brain. The rate at which the brain recovers from serotonergic changes is unclear. One study demonstrated lasting serotonergic changes in some animals exposed to MDMA.[71] Other studies have suggested that the brain may recover from serotonergic damage.[72][73][74]

It is thought that MDMA's metabolites play a large role in the uncertain levels of neurotoxicity. For example, a metabolite of MDMA called alpha-Methyldopamine (α-Me-DA, which is known to be toxic to dopamine neurons[75][18]) was thought believed to be involved in the toxicity of MDMA to serotonin receptors.

However, one study found this to not be the case as direct administration of α-Me-DA did not cause neurotoxicity.[18] Additionally, MDMA injected directly into the brain was found to not be toxic, implying a metabolite is responsible for the toxicity when MDMA is administered via insufflation or oral consumption.[18]

This study found that although α-Me-DA is involved, it is a further metabolite of α-Me-DA involving glutathione that is primarily responsible for the selective damage to 5-HT receptors triggered by MDMA/MDA.[18]This metabolite forms in higher concentrations when core temperature is elevated. It is taken up into serotonin receptors by its transporters and metabolized by MAO-B into a reactive oxygen species which can cause neurological damage.[18][76]

Retracted article on dopaminergic neurotoxicity of MDMA

Severe dopaminergic neurotoxicity in primates after a common recreational dose regimen of MDMA[77] is an article by George A. Ricaurte which was published in September 2002 in the peer-reviewed journal Science, one of the world's top academic journals. It was later retracted; instead of using MDMA, methamphetamine had been used in the test.


Long-term heavy use of MDMA has been shown to be cardiotoxic and may lead to valvulopathy (heart valve damage) through its actions on the 5-HT2B receptor.[78][76]

In one study, 28% of long-term users (2-3 doses per week for a mean of 6 years, mean of age 24.3 years) had developed clinically evident valvular heart disease.[79]

It is strongly recommended that one use harm reduction practices when using this substance.

Dependence and abuse potential

As with other stimulants, the chronic use of MDMA can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if one suddenly stops their usage.

Tolerance to many of the effects of MDMA develops with prolonged and repeated use. This results in users having to administer increasingly larger doses to achieve the same effects.

Upon a single administration, it takes about 1 month for the tolerance to be reduced to half and 2.5 months to be back at baseline (in the absence of further consumption).

MDMA exhibits cross-tolerance with all dopaminergic and serotonergic stimulants, meaning that after the consumption of MDMA all stimulants will have a reduced effect.

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • SSRIs and SNRIs - may dampen the the desired psychological effects of MDMA while retaining the same level of undesirable physiological side-effects.[80][81] But unlike common belief it doesn't cause serotonin syndrome.[citation needed]
  • 25x-NBOMe - Due to the highly unpredictable and physically straining effects of 25x-NBOMe, combinations with MDMA are strongly discouraged.
  • Protease Inhibitors - Certain HIV medications like Ritonavir or Cobicistat contain protease inhibitors, that cause the liver to process MDMA slower resulting in longer and stronger effects, which causes more harm to the liver and might cause overdosing. A lower dose is recommended. [82]
  • 5-MeO-xxT - 5-MeO tryptamines are considered to be unpredictable and should be mixed with MDMA with care.
  • Alcohol - Both MDMA and alcohol cause dehydration and bodily strain. Approach this combination with caution, moderation and sufficient hydration. More than a small amount of alcohol will dull the euphoria of MDMA.
  • Cocaine - Cocaine blocks some of the desirable effects of MDMA while increasing the risk of heart attack.[citation needed]
  • DOx - The combined stimulating effects of DOx and MDMA can become overbearing, particularly during the come-up phase. Additionally, coming down on the MDMA while the DOx is still active can produce significant anxiety and bodily discomfort.
  • GHB/GBL - Large amounts of GHB/GBL may overwhelm the effects of MDMA on the comedown and place the user at risk of sudden loss of consciousness.
  • MXE - There have been reports of concerning serotonergic interactions when the two are taken at the same time, but MXE taken to the end of an MDMA experience does not appear to cause the same issues.
  • PCP - PCP with MDMA may increase the risk of excessive stimulation, mania, and psychosis.
  • Tramadol - Tramadol is well-documented to lower the seizure threshold[83] and this risk is especially elevated when tramadol is taken with MDMA.

Serotonin syndrome risk

Combinations with the following substances can lead to dangerously high serotonin levels. Serotonin syndrome requires immediate medical attention and can be fatal if left untreated.

  • MAOIs such as syrian rue, banisteriopsis caapi, phenelzine, selegiline, and moclobemide[84] - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with MDMA will lead to hypertensive crises.
  • Serotonin releasers such as MDMA, 4-FA, methamphetamine, methylone and αMT
  • AMT
  • 2C-T-x
  • DXM
  • 5-HTP - 5-HTP is a supplement that acts as a precursor for serotonin. It is sometimes recommended to be used after MDMA experiences to try to restore depleted serotonin reserves. However, taking 5-HTP shortly before or with MDMA may cause excessive serotonin levels in the brain, which can lead to serotonin syndrome.[85] As a result, it is advised to wait until the day after the MDMA has been used before consuming 5-HTP.

Legal status

Internationally, MDMA was added to the UN Convention on Psychotropic Substances as a Schedule I controlled substance in February 1986.[86]

  • Australia: MDMA is a Schedule 8 (Controlled Drugs) drug in Australia, starting July 1st 2023. [87] Personal quantities under 1.5 grams (or 5 single doses, such as when in tablet form) are decriminalized in the Australian Capital Territory (ACT) as of 28 October 2023.[88]
  • Austria: MDMA is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[89]
  • Belgium: MDMA is illegal to possess, produce and sell in Belgium.[90]
  • Brazil: MDMA is illegal to possess, produce and sell under Portaria SVS/MS nº 344.[91]
  • Canada: MDMA is a Schedule I drug in Canada.[92]
  • Denmark: MDMA is illegal to possess, produce and sell in Denmark.[93]
  • Egypt: MDMA is a Schedule III drug in Egypt.[citation needed]
  • Finland: MDMA is illegal to possess, produce and sell in Finland.[citation needed]
  • Germany: MDMA is controlled under Anlage I BtMG (Narcotics Act, Schedule I)[94] as of August 1, 1986.[95] It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.[96]
  • Latvia: MDMA is a Schedule I drug in Latvia.[97]
  • Luxembourg: MDMA is a prohibited substance.[98]
  • The Netherlands: MDMA is illegal to possess, produce and sell in the Netherlands.[99]
  • New Zealand: MDMA is a Class B1 drug in New Zealand.[100]
  • Norway: MDMA is illegal to possess, produce and sell in Norway.[citation needed]
  • Portugal: MDMA is illegal to produce, sell or trade in Portugal. However, since 2001, individuals found in possession of small quantities (up to 1 gram) are considered sick individuals instead of criminals. The drugs are confiscated and the suspects may be forced to attend a dissuasion session at the nearest CDT (Commission for the Dissuasion of Drug Addiction) or pay a fine, in most cases.[101]
  • Russia: MDMA is classified as a Schedule I prohibited substance.[102]
  • Sweden: MDMA is illegal to possess, produce and sell in Sweden.[citation needed]
  • Switzerland: MDMA is a controlled substance specifically named under Verzeichnis D.[103]
  • United Kingdom: MDMA is a Class A drug in the UK.[104]
  • United States: MDMA is classified as a Schedule I drug under the Controlled Substance Act. This means it is illegal to manufacture, buy, possess, process, or distribute without a license from the Drug Enforcement Administration (DEA).[105]
  • Czech Republic: MDMA is a Schedule I controlled substance.[106]

See also

External links

Harm reduction


  1. 1.0 1.1 1.2 Freudenmann, Roland W.; Öxler, Florian; Bernschneider-Reif, Sabine (2006). "The origin of MDMA (ecstasy) revisited:the true story reconstructed from the original documents". Addiction. 101 (9): 1241–1245. doi:10.1111/j.1360-0443.2006.01511.x. ISSN 1360-0443. 
  2. 2.0 2.1 2.2 Shulgin, Alexander; Shulgin, Ann (1991). "Chapter 12". PiHKAL: A Chemical Love Story. Part 1. Transform Press. pp. 66–74. ISBN 0963009605. 
  3. Merck and Ecstasy / MDMA 
  4. The Global Drug Survey 2014 findings 
  5. World Health Organization, ed. (2004). Neuroscience of psychoactive substance use and dependence. World Health Organization. ISBN 9789241562355. 
  6. Multidisciplinary Association for Psychedelic Studies (2022), A Placebo-controlled, Randomized, Blinded, Dose Finding Phase 2 Pilot Safety Study of MDMA-assisted Therapy for Social Anxiety in Autistic Adults, 
  7. MDMA-Assisted Therapy for Anxiety Associated with Life-Threatening Illness (MDA-1) 
  8. Meyer, J. S. (21 November 2013). "3,4-methylenedioxymethamphetamine (MDMA): current perspectives". Substance Abuse and Rehabilitation. 4: 83–99. doi:10.2147/SAR.S37258. 
  9. Parrott, A. C. (March 2014). "The potential dangers of using MDMA for psychotherapy". Journal of Psychoactive Drugs. 46 (1): 37–43. doi:10.1080/02791072.2014.873690. ISSN 0279-1072. 
  10. Meyer, J. S. (2013). "3,4-methylenedioxymethamphetamine (MDMA): current perspectives". Substance Abuse and Rehabilitation. 4: 83–99. doi:10.2147/SAR.S37258. ISSN 1179-8467. 
  11. Greene, S. L., Kerr, F., Braitberg, G. (October 2008). "Review article: amphetamines and related drugs of abuse". Emergency medicine Australasia: EMA. 20 (5): 391–402. doi:10.1111/j.1742-6723.2008.01114.x. ISSN 1742-6723. 
  12. Nestler, E. J., Hyman, S. E., Malenka, R. C. (2009). Molecular neuropharmacology: a foundation for clinical neuroscience (2nd ed ed.). McGraw-Hill Medical. ISBN 9780071481274. 
  13. Gouzoulis-Mayfrank, E., Daumann, J. (2009). "Neurotoxicity of drugs of abuse--the case of methylenedioxyamphetamines (MDMA, ecstasy), and amphetamines". Dialogues in Clinical Neuroscience. 11 (3): 305–317. ISSN 1294-8322. 
  14. 14.0 14.1 Karch, Steven (2011). "A Historical Review of MDMA". The Open Forensic Science Journal. 4: 20–24. doi:10.2174/1874402801104010020. ISSN 1874-4028. 
  15. 15.0 15.1 Sessa, B. (2017). The Psychedelic Renaissance: Reassessing the Role of Psychedelic Drugs in 21st Century Psychiatry and Society. Muswell Hill Press. ISBN 9781908995278. 
  16. Young, Francis L. (May 22, 1968). "In The Matter Of MDMA Scheduling: Opinion And Recommended Ruling, Findings Of Fact, Conclusions Of Law And Decision Of Administrative Law Judge On Issues Two Through Seven" (PDF). Multidisciplinary Association for Psychedelic Studies. Retrieved November 14, 2019. 
  17. "3,4-Methylenedioxymethamphetamine". Hazardous Substances Data Bank. National Library of Medicine. 28 August 2008. Retrieved 22 August 2014.
  18. 18.00 18.01 18.02 18.03 18.04 18.05 18.06 18.07 18.08 18.09 18.10 Miller, G. M. (January 2011). "The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity: TAAR1 regulation of monoaminergic activity". Journal of Neurochemistry. 116 (2): 164–176. doi:10.1111/j.1471-4159.2010.07109.x. ISSN 0022-3042.  Cite error: Invalid <ref> tag; name "Miller2011" defined multiple times with different content
  19. 19.0 19.1 19.2 Eiden, L. E., Weihe, E. (January 2011). "VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse: VMAT2 and addiction". Annals of the New York Academy of Sciences. 1216 (1): 86–98. doi:10.1111/j.1749-6632.2010.05906.x. ISSN 0077-8923. 
  20. Fitzgerald, J. L., Reid, J. J. (November 1990). "Effects of methylenedioxymethamphetamine on the release of monoamines from rat brain slices". European Journal of Pharmacology. 191 (2): 217–220. doi:10.1016/0014-2999(90)94150-V. ISSN 0014-2999. 
  21. Eiden, L. E., Weihe, E. (January 2011). "VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse: VMAT2 and addiction". Annals of the New York Academy of Sciences. 1216 (1): 86–98. doi:10.1111/j.1749-6632.2010.05906.x. ISSN 0077-8923. 
  22. Bogen, I. L., Haug, K. H., Myhre, O., Fonnum, F. (September 2003). "Short- and long-term effects of MDMA ("ecstasy") on synaptosomal and vesicular uptake of neurotransmitters in vitro and ex vivo". Neurochemistry International. 43 (4–5): 393–400. doi:10.1016/S0197-0186(03)00027-5. ISSN 0197-0186. 
  23. Nelson, L., Goldfrank, L. R., eds. (2011). Goldfrank’s toxicologic emergencies (9th ed ed.). McGraw-Hill Medical. ISBN 9780071605939. 
  24. Battaglia, G., Brooks, B. P., Kulsakdinun, C., De Souza, E. B. (April 1988). "Pharmacologic profile of MDMA (3,4-methylenedioxymethamphetamine) at various brain recognition sites". European Journal of Pharmacology. 149 (1–2): 159–163. doi:10.1016/0014-2999(88)90056-8. ISSN 0014-2999. 
  25. Lyon, RobertA., Glennon, RichardA., Titeler, M. (April 1986). "3,4-Methylenedioxymethamphetamine (MDMA): Stereoselective interactions at brain 5-HT1 and 5-HT2 receptors". Psychopharmacology. 88 (4). doi:10.1007/BF00178519. ISSN 0033-3158. 
  26. Nash, J. F., Roth, B. L., Brodkin, J. D., Nichols, D. E., Gudelsky, G. A. (August 1994). "Effect of the R(−) and S(+) isomers of MDA and MDMA on phosphotidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors". Neuroscience Letters. 177 (1–2): 111–115. doi:10.1016/0304-3940(94)90057-4. ISSN 0304-3940. 
  27. Setola, V., Hufeisen, S. J., Grande-Allen, K. J., Vesely, I., Glennon, R. A., Blough, B., Rothman, R. B., Roth, B. L. (June 2003). "3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy") Induces Fenfluramine-Like Proliferative Actions on Human Cardiac Valvular Interstitial Cells in Vitro". Molecular Pharmacology. 63 (6): 1223–1229. doi:10.1124/mol.63.6.1223. ISSN 0026-895X. 
  28. Betzler, F., Viohl, L., Romanczuk-Seiferth, N. (January 2017). Foxe, J., ed. "Decision-making in chronic ecstasy users: a systematic review". European Journal of Neuroscience. 45 (1): 34–44. doi:10.1111/ejn.13480. ISSN 0953-816X. 
  29. Matsumoto, R. R. (July 2009). "Targeting sigma receptors: novel medication development for drug abuse and addiction". Expert Review of Clinical Pharmacology. 2 (4): 351–358. doi:10.1586/ecp.09.18. ISSN 1751-2433. 
  30. 30.0 30.1 Kalant, H. (2 October 2001). "The pharmacology and toxicology of "ecstasy" (MDMA) and related drugs". CMAJ: Canadian Medical Association Journal. 165 (7): 917–928. ISSN 0820-3946. 
  31. Bexis, S., Docherty, J. R. (April 2006). "Effects of MDMA, MDA and MDEA on blood pressure, heart rate, locomotor activity and body temperature in the rat involve α -adrenoceptors: MDMA on rat vascular and temperature responses". British Journal of Pharmacology. 147 (8): 926–934. doi:10.1038/sj.bjp.0706688. ISSN 0007-1188. 
  32. Liechti, M. E. (31 October 2014). "Effects of MDMA on body temperature in humans". Temperature: Multidisciplinary Biomedical Journal. 1 (3): 192–200. doi:10.4161/23328940.2014.955433. ISSN 2332-8940. 
  33. 3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy) and Driving Impairment 
  35. Greer, G. R., Tolbert, R. (December 1998). "A method of conducting therapeutic sessions with MDMA". Journal of Psychoactive Drugs. 30 (4): 371–379. doi:10.1080/02791072.1998.10399713. ISSN 0279-1072. 
  36. (1995), A Dose/Response Human Pilot Study – Safety and Efficacy of MDMA in Modification of Physical Pain and Psychological Distress in End-Stage Cancer Patients, retrieved 2 August 2022 
  37. Buffum, John; Moser, Charles (October 1986). "MDMA and Human Sexual Function". Journal of Psychoactive Drugs. 18 (4): 355–359. doi:10.1080/02791072.1986.10472369. ISSN 0279-1072. PMID 2880951. 
  38. Zemishlany, Z.; Aizenberg, D.; Weizman, A. (March 2001). "Subjective effects of MDMA ('Ecstasy') on human sexual function". European Psychiatry. 16 (2): 127–130. doi:10.1016/s0924-9338(01)00551-x. ISSN 0924-9338. PMID 11311179.  Unknown parameter |s2cid= ignored (help)
  39. Dinis-Oliveira, R. J., Caldas, I., Carvalho, F., Magalhães, T. (1 October 2010). "Bruxism after 3,4-methylenedioxymethamphetamine (ecstasy) abuse". Clinical Toxicology. 48 (8): 863–864. doi:10.3109/15563650.2010.489903. ISSN 1556-3650. 
  40. Urban Dictionary: gurning 
  41. Parrott, Andy C.; Milani, Raffaella M.; Parmar, Rishee; Turner, John J. (2001-09-11). "Recreational ecstasy/MDMA and other drug users from the UK and Italy: psychiatric symptoms and psychobiological problems". Psychopharmacology. 159 (1): 77–82. doi:10.1007/s002130100897. ISSN 0033-3158. PMID 11797073.  Unknown parameter |s2cid= ignored (help)
  42. Passie, Torsten; Hartmann, Uwe; Schneider, Udo; Emrich, Hinderk M.; Krüger, Tillmann H.C. (January 2005). "Ecstasy (MDMA) mimics the post-orgasmic state: Impairment of sexual drive and function during acute MDMA-effects may be due to increased prolactin secretion". Medical Hypotheses. 64 (5): 899–903. doi:10.1016/j.mehy.2004.11.044. ISSN 0306-9877. PMID 15780482. 
  43. Topp, Libby; Hando, Julie; Dillon, Paul; Roche, Ann; Solowij, Nadia (June 1999). "Ecstasy use in Australia: patterns of use and associated harm". Drug and Alcohol Dependence. 55 (1–2): 105–115. doi:10.1016/s0376-8716(99)00002-2. ISSN 0376-8716. PMID 10402155. 
  44. "MDMA Auswertung 2018" [MDMA Evaluation 2018] (PDF). (in German). Sozialdepartement Zürich. 2018. Retrieved January 18, 2020. 
  45. Effects Relationship for MDMA from Analyzed Samples (DIMS 2011) 
  46. Green, A. R., Mechan, A. O., Elliott, J. M., O’Shea, E., Colado, M. I. (1 September 2003). "The Pharmacology and Clinical Pharmacology of 3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy")". Pharmacological Reviews. 55 (3): 463–508. doi:10.1124/pr.55.3.3. ISSN 0031-6997. 
  47. Kahn, D. E., Ferraro, N., Benveniste, R. J. (15 December 2012). "3 cases of primary intracranial hemorrhage associated with "Molly", a purified form of 3,4-methylenedioxymethamphetamine (MDMA)". Journal of the Neurological Sciences. 323 (1): 257–260. doi:10.1016/j.jns.2012.08.031. ISSN 0022-510X. 
  48. Shulgin Index, p811
  50. "MDMA Auswertung 2018" [MDMA Evaluation 2018] (PDF). (in German). Sozialdepartement Zürich. 2018. Retrieved January 18, 2020. 
  51. 51.0 51.1 Mithoefer, M. C., Wagner, M. T., Mithoefer, A. T., Jerome, L., Martin, S. F., Yazar-Klosinski, B., Michel, Y., Brewerton, T. D., Doblin, R. (January 2013). "Durability of improvement in post-traumatic stress disorder symptoms and absence of harmful effects or drug dependency after 3,4-methylenedioxymethamphetamine-assisted psychotherapy: a prospective long-term follow-up study". Journal of Psychopharmacology. 27 (1): 28–39. doi:10.1177/0269881112456611. ISSN 0269-8811. 
  52. Wan, W. (2017), Ecstasy could be ‘breakthrough’ therapy for soldiers, others suffering from PTSD, retrieved August 29, 2017 
  53. Feduccia, A. A., Holland, J., Mithoefer, M. C. (February 2018). "Progress and promise for the MDMA drug development program". Psychopharmacology. 235 (2): 561–571. doi:10.1007/s00213-017-4779-2. ISSN 1432-2072. 
  54. Inverse: MDMA Steps Closer to FDA Approval as a Drug, but Now it Needs to Leap, 2016 
  55. Curry, D. W., Young, M. B., Tran, A. N., Daoud, G. E., Howell, L. L. (January 2018). "Separating the agony from ecstasy: R(–)-3,4-methylenedioxymethamphetamine has prosocial and therapeutic-like effects without signs of neurotoxicity in mice". Neuropharmacology. 128: 196–206. doi:10.1016/j.neuropharm.2017.10.003. ISSN 0028-3908. 
  56. Nutt DJ, King LA, Phillips LD (November 2010). "Drug harms in the UK: a multicriteria decision analysis". Lancet. 376 (9752): 1558–1565. CiteSeerX accessible. doi:10.1016/S0140-6736(10)61462-6. PMID 21036393.  Unknown parameter |s2cid= ignored (help)
  57. Nutt, D., King, L. A., Saulsbury, W., Blakemore, C. (March 2007). "Development of a rational scale to assess the harm of drugs of potential misuse". The Lancet. 369 (9566): 1047–1053. doi:10.1016/S0140-6736(07)60464-4. ISSN 0140-6736. 
  58. Nimmo, S. M., Kennedy, B. W., Tullett, W. M., Blyth, A. S., Dougall, J. R. (October 1993). "Drug-induced hyperthermia". Anaesthesia. 48 (10): 892–895. doi:10.1111/j.1365-2044.1993.tb07423.x. ISSN 0003-2409. 
  59. Malberg, J. E., Seiden, L. S. (1 July 1998). "Small changes in ambient temperature cause large changes in 3,4-methylenedioxymethamphetamine (MDMA)-induced serotonin neurotoxicity and core body temperature in the rat". The Journal of Neuroscience: The Official Journal of the Society for Neuroscience. 18 (13): 5086–5094. ISSN 0270-6474. 
  60. Wolff, K., Tsapakis, E. M., Winstock, A. R., Hartley, D., Holt, D., Forsling, M. L., Aitchison, K. J. (May 2006). "Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population". Journal of Psychopharmacology. 20 (3): 400–410. doi:10.1177/0269881106061514. ISSN 0269-8811. 
  61. Nadesan, K., Kumari, C., Afiq, M. (1 August 2017). "Dancing to death: A case of heat stroke". Journal of Forensic and Legal Medicine. 50: 1–5. doi:10.1016/j.jflm.2017.05.008. ISSN 1752-928X. 
  68. Bora, F., Yılmaz, F., Bora, T. (November 2016). "Ecstasy (MDMA) and its effects on kidneys and their treatment: a review". Iranian Journal of Basic Medical Sciences. 19 (11): 1151–1158. ISSN 2008-3866. 
  69. Inman, D. S., Greene, D. (January 2003). "'The agony and the ecstasy': acute urinary retention after MDMA abuse". BJU International. 91 (1): 123–123. doi:10.1046/j.1464-410X.2003.04018.x. ISSN 1464-4096. 
  70. Brvar, M., Kozelj, G., Osredkar, J., Mozina, M., Gricar, M., Bunc, M. (October 2004). "Polydipsia as another mechanism of hyponatremia after "ecstasy" (3,4 methyldioxymethamphetamine) ingestion". European Journal of Emergency Medicine: Official Journal of the European Society for Emergency Medicine. 11 (5): 302–304. doi:10.1097/00063110-200410000-00014. ISSN 0969-9546. 
  71. Fischer, C., Hatzidimitriou, G., Wlos, J., Katz, J., Ricaurte, G. (August 1995). "Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy")". The Journal of Neuroscience: The Official Journal of the Society for Neuroscience. 15 (8): 5476–5485. ISSN 0270-6474. 
  72. Scheffel, U., Szabo, Z., Mathews, W. B., Finley, P. A., Dannals, R. F., Ravert, H. T., Szabo, K., Yuan, J., Ricaurte, G. A. (June 1998). <183::AID-SYN9>3.0.CO;2-3 "In vivo detection of short- and long-term MDMA neurotoxicity?a positron emission tomography study in the living baboon brain". Synapse. 29 (2): 183–192. doi:10.1002/(SICI)1098-2396(199806)29:2<183::AID-SYN9>3.0.CO;2-3. ISSN 0887-4476. 
  73. Reneman, L., Lavalaye, J., Schmand, B., Wolff, F. A. de, Brink, W. van den, Heeten, G. J. den, Booij, J. (1 October 2001). "Cortical Serotonin Transporter Density and Verbal Memory in Individuals Who Stopped Using 3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy"): Preliminary Findings". Archives of General Psychiatry. 58 (10): 901. doi:10.1001/archpsyc.58.10.901. ISSN 0003-990X. 
  74. Selvaraj, S., Hoshi, R., Bhagwagar, Z., Murthy, N. V., Hinz, R., Cowen, P., Curran, H. V., Grasby, P. (April 2009). "Brain serotonin transporter binding in former users of MDMA ('ecstasy')". British Journal of Psychiatry. 194 (4): 355–359. doi:10.1192/bjp.bp.108.050344. ISSN 0007-1250. 
  75. Perfetti, X., O’Mathúna, B., Pizarro, N., Cuyàs, E., Khymenets, O., Almeida, B., Pellegrini, M., Pichini, S., Lau, S. S., Monks, T. J., Farré, M., Pascual, J. A., Joglar, J., Torre, R. de la (July 2009). "Neurotoxic thioether adducts of 3,4-methylenedioxymethamphetamine identified in human urine after ecstasy ingestion". Drug Metabolism and Disposition: The Biological Fate of Chemicals. 37 (7): 1448–1455. doi:10.1124/dmd.108.026393. ISSN 1521-009X. 
  76. 76.0 76.1 Elangbam, C. S. (October 2010). "Drug-induced Valvulopathy: An Update". Toxicologic Pathology. 38 (6): 837–848. doi:10.1177/0192623310378027. ISSN 0192-6233. 
  77. Ricaurte GA, Yuan J, Hatzidimitriou G, Cord BJ, McCann UD (September 2002). "Severe dopaminergic neurotoxicity in primates after a common recreational dose regimen of MDMA ("ecstasy")". Science. 297 (5590): 2260–3. Bibcode:2002Sci...297.2260R. doi:10.1126/science.1074501. PMID 12351788.  Unknown parameter |s2cid= ignored (help)
  78. Rothman, R. B., Baumann, M. H., Savage, J. E., Rauser, L., McBride, A., Hufeisen, S. J., Roth, B. L. (5 December 2000). "Evidence for Possible Involvement of 5-HT 2B Receptors in the Cardiac Valvulopathy Associated With Fenfluramine and Other Serotonergic Medications". Circulation. 102 (23): 2836–2841. doi:10.1161/01.CIR.102.23.2836. ISSN 0009-7322. 
  79. Droogmans, S., Cosyns, B., D’haenen, H., Creeten, E., Weytjens, C., Franken, P. R., Scott, B., Schoors, D., Kemdem, A., Close, L., Vandenbossche, J.-L., Bechet, S., Van Camp, G. (1 November 2007). "Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease". The American Journal of Cardiology. 100 (9): 1442–1445. doi:10.1016/j.amjcard.2007.06.045. ISSN 0002-9149. 
  80. Ewens, H. (2017), Everything You Need to Know About Mixing MDMA and Antidepressants 
  81. Dobry, Y., Rice, T., Sher, L. (2013). "Ecstasy use and serotonin syndrome: a neglected danger to adolescents and young adults prescribed selective serotonin reuptake inhibitors". International Journal of Adolescent Medicine and Health. 25 (3): 193–199. doi:10.1515/ijamh-2013-0052. ISSN 0334-0139. 
  82. Harrington, Robert D.; Woodward, Jane A.; Hooton, Thomas M.; Horn, John R. (1999-10-11). "Life-Threatening Interactions Between HIV-1 Protease Inhibitors and the Illicit Drugs MDMA and γ-Hydroxybutyrate". Archives of Internal Medicine. American Medical Association (AMA). 159 (18): 2221. doi:10.1001/archinte.159.18.2221. ISSN 0003-9926. 
  83. Talaie, H.; Panahandeh, R.; Fayaznouri, M. R.; Asadi, Z.; Abdollahi, M. (2009). "Dose-independent occurrence of seizure with tramadol". Journal of Medical Toxicology. 5 (2): 63–67. doi:10.1007/BF03161089. eISSN 1937-6995. ISSN 1556-9039. OCLC 163567183. PMC 3550327Freely accessible. PMID 19415589. 
  84. Gillman, P. K. (October 2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210. ISSN 0007-0912. 
  85. Silins, E.; Copeland, J.; Dillon, P. (2007). "Qualitative Review of Serotonin Syndrome, Ecstasy (MDMA) and the use of Other Serotonergic Substances: Hierarchy of Risk". Australian and New Zealand Journal of Psychiatr. 41 (8): 649–655. doi:10.1080/00048670701449237. eISSN 1440-1614. ISSN 0004-8674. PMID 17620161. 
  86. "Decision to place MDMA into Schedule I" (PDF). UNODC. Commission on Narcotic Drugs. 11 February 1986. Retrieved November 11, 2019. 
  87. Australian MDMA and Psilocybin, new laws., 2023 
  89. Suchtgiftverordnung, aktuelle Fassung 
  90. EMCDDA Country legal profiles - Belgium |
  91. List of controlled substances: Portaria SVS/MS nº 344 (Portuguese) |
  92. Branch, L. S. (2022), Consolidated federal laws of canada, Controlled Drugs and Substances Act 
  93. EMCDDA Country legal profiles - Denmark |
  94. "Anlage I BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 18, 2019. 
  95. "Zweite Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften" (in German). Bundesanzeiger Verlag. Retrieved December 18, 2019. 
  96. "§ 29 BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 18, 2019. 
  97. Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem (3,4-Metilēndioksifeniletānamīni) 
  98. Règlement grand-ducal du 13 juin 1986 complétant l'annexe du règlement grand-ducal du 20 mars 1974 concernant certaines substances psychotropes. |
  99. Opiumwet |,15700022,15700186,15700191,15700256,15700259,15700262,15700265,15700271,15700283&usg=ALkJrhg0a81esxOUix1UMvvAvbVALDP2-Q#BijlageI
  100. Misuse of Drugs Act 1975 No 116 (as at 01 July 2022), Public Act – New Zealand Legislation 
  101. Greenwald, G. (2009), Drug Decriminalization in Portugal: Lessons for Creating Fair and Successful Drug Policies, Social Science Research Network 
  102. Resolution of the Government of the Russian Federation |,0&rnd=0.41568319511755825#047741519652799347
  103. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  104. Misuse of Drugs Act 1971 
  105. DEA / Drug Scheduling |